Acute sepsis is characterized by an accelerated catabolism of somatic proteins, an increased rate of oxidation and transamination of branched-chain amino acids within muscle, an enhanced formation of lactic acid, alanine and glutamine in muscle, an enhanced flux of these substrates from muscle to liver, and an acceleration of the synthesis and release of glucose from the liver. Endocrine responses which influence these metabolic changes include an enhanced secretion of both insulin and glucagon from pancreatic islet cells and a resultant decrease in the molar ratio of insulin to glucagon in plasma. The secretion of the adrenal glucocorticoids and growth hormone are increased as may be the secretion of catecholamines. The accelerated release of glucose from the liver is generally accompanied by an increase in glucose pool size and an increase in the rate of glucose utilization as a cellular fuel. The hormonal, enzymatic, and substrate interrelationships within the liner combine in their effects to inhibit Ketogenesis and stimulate hepatic lipogenesis during acute sepsis.